An Investigation of Repetition and Language …caram/PDFs/1981_Caramazza_Basili...236 CARAMAZZA ET...

BRAIN AND LANGUAGE 14, 235-271 (1981)

An Investigation of Repetition and Language Processing in a Case of Conduction Aphasia

ALFONSO CARAMAZZA

The Johns Hopkins University

ANNAMARIA G. BASILI AND JERRY J. KOLLER

Fort Howard Veterans Administration Medical Center

AND

RITA SLOAN BERNDT

The Johns Hopkins University

A study is reported of a single case of conduction aphasia. A battery of tasks designed to investigate the parameters of the patient’s severe repetition deficit is supplemented by tests of several language functions. The results provide extensive information on a wide range of the patient’s language abilities and are used to evaluate the adequacy of four models that have been offered to account for conduction aphasia. An argument is made in support of the suggestion that the syndrome of conduction aphasia should be divided into two subgroups based on patients’ ability to select and realize phonemes in speech output. It is con- cluded that the best explanation for the disorder of patients with repetition deficit but without significant speech output problems is the hypothesis that repetition ability is compromised by a pathological limitation of auditory-verbal short-term memory. This hypothesis is extended to account for the pattern of results obtained in the language tasks.

In 1874 Carl Wernicke predicted the syndrome of conduction aphasia on the basis of his neuroanatomical model of the distribution and interaction of language functions in the dominant hemisphere. Lichtheim’s

The research reported here was supported by NIH Research Grant 14099 to the Johns Hopkins University. We would like to thank John Hart for designing the oral reading tasks, and for his help in testing the patients on several of the tasks. We would also like to thank Edgar Zurif for his helpful comments on an earlier draft of this paper. Address reprint requests to Dr. Alfonso Caramazza, Department of Psychology, The Johns Hopkins University, Baltimore, MD 21218.

235

0093-934X/81/060235-37$02.00/0 Copyright 0 1981 by Academic Press, Inc.

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236 CARAMAZZA ET AL.

(1884) clinical description of the first case of conduction aphasia provided a verification of Wernicke’s prediction, as well as an elaboration of the syndrome to include a deficit of repetition ability as a major symptom. Numerous cases of conduction aphasia have been reported in the neu- rological and neuropsychological literature since Lichtheim’s original report (see Benson, Sheremata, Bouchard, Segarra, Price, & Geschwind, 1973; Green & Howes, 1977). There now appears to be some agreement that the lesion site in the left hemisphere associated with conduction aphasia is the posterior third of the first temporal gyrus and the supra- marginal gyrus, with possible involvement of the arcuate fasciculus (Benson et al., 1973). There is less agreement on the underlying functional features: a marked and disproportionate difficulty repeating spoken words; relatively good comprehension (on clinical testing) and fluent speech; occasional word-finding difficulties; the occurrence of occasional literal or verbal paraphasias; difficulties in spelling and writing; and some problems with oral reading.

The explanation offered by Wernicke and Lichtheim for the clinical features of conduction aphasia rests on the assumption that specific components of language representation (e.g., sound images) are orga- nized in cortical centers that are connected to one another; language functions such as speaking and comprehension require the normal par- ticipation of these various cortical centers. Conduction aphasia was assumed to be a “disconnection” syndrome in which Broca’s area (center for articulatory gestures) is severed from Wernicke’s area (center for sound images), resulting in a dissociation of two components of a word. Since Broca’s and Wernicke’s areas are presumably spared, the patient should have normal comprehension and articulatory ability. His language deficit should be restricted to occasional word choice difficulties in spontaneous speech and a disproportionate problem with repetition (see also Geschwind, 1965).

This view of conduction aphasia did not go unchallenged. Freud (1891) and later Goldstein (1948) criticized Wernicke’s disconnection model. While accepting the existence of the clinical picture offered for conduction aphasia, Goldstein strongly disagreed on the interpretation of the mechanisms responsible for the deficit. He assumed that conduction aphasia (which he renamed “central aphasia”) involved a disruption of the mechanisms of “inner speech”; consequently, all speech performance should be affected to some extent, with repetition especially impaired. Hecaen and his collaborators have further refined and elaborated Goldstein’s interpretation of conduction aphasia to focus on the encoding of inner speech forms into the motor output program (Dubois, Hecaen, Angelergues, de Chatelier, & Marcie, 1964; Hecaen & Albert, 1978; Hecaen, Dell, & Roger, 1955). Other interpretations of conduction aphasia have been offered that differ in important ways from the dis-

CONDUCTION APHASIA 237

connection model (e.g., Alajouanine & Lhermitte, 1964; Kinsbourne, 1972; Kleist, 1916). A feature shared by all of these hypotheses is that the disproportionate repetition deficit that is the cardinal feature of conduction aphasia is regarded as a symptom secondary to a more general language deficit.

Over the last decade Warrington and Shallice have suggested that, at least in some cases, the symptoms of conduction aphasia result from an impairment of auditory-verbal short-term memory @TM) (Shallice & Butterworth, 1977; Shallice & Warrington, 1970, 1974, 1977; Warrington, Logue, & Pratt, 1971; Warrington & Shallice, 1969, 1972). In a series of detailed analyses of several case studies, Warrington and Shallice have provided compelling evidence and arguments to support this thesis. A number of critical replies have been published (Kinsbourne, 1972; Strub & Gardner, 1974, Tzortzis & Albert, 1974), and debate continues over whether or not conduction aphasia should be considered primarily a disorder of memory. This debate comprises the primary theoretical focus of the studies reported here. The details of the STM-deficit hypothesis, and the points raised by its detractors, will be discussed in detail as the data are presented.

In this paper we report a case study of a relatively pure case of conduction aphasia. After a brief presentation of the patient’s history and his performance on various standardized tests, we will present some data on his repetition ability. Discussion of repetition is followed by an analysis of his ability to read, to comprehend, and to produce language. An assessment of the patient’s performance on these latter language functions is reported in order to evaluate the hypothesis that the repetition deficit in this patient is secondary to a language processing disorder. Stated differently, a detailed picture of the patient’s language and repetition performance is necessary in order to impose reasonable constraints on a model of conduction aphasia.

CASE HISTORY

MC is a black male who was 58 years old at the time this study was initiated. He is a high school graduate who was employed for 30 years as a machinist. In June of 1976 MC suffered a left-cerebrovascular ac- cident, which resulted initially in a mild right-sided hemiparesis and “moderately severe mixed aphasia.”

The patient was followed as an outpatient in the Department of Au- diology and Speech pathology at the Fort Howard Veterans Adminis- tration Medical Center, and by the summer of 1978 he had progressed to a condition in which his overall language functions were judged to be only mildly impaired on clinical testing. He was classified at that time as a conduction aphasic on the basis of the Boston Diagnostic Aphasia Examination (Goodglass & Kaplan, 1972).


Audiological examination revealed a mild conductive hearing loss, with residual capacities judged to be adequate for speech. MC’s visual acuity is corrected, with no visual field impairments.

On first impression, MC’s language disability appears to be minor. He is attentive in social situations and seems to communicate without difficulty in casual conversation. However, close scrutiny of his verbal output in structured conversation reveals moderate word-finding difficulties and occasional paragrammatism. MC’s comprehension of sentences is quite impaired when assessed rigorously, and, of course, he exhibits a striking inability to repeat words presented aurally. Results of some standard clinical tests are presented in Table 1. It is evident that MC’s comprehension of single words (Peabody; BDAE Word Dis- crimination and Body Part Identification subtests) is spared relative to his comprehension of sentences (Token Test; BDAE Commands subtest). Other subtests of the Boston Diagnostic rule out his classification as a Wernicke’s or an anemic aphasic.

CT scan reveals a focal lesion in the left posterior and superior temporal

TABLE 1 PERFORMANCE OF PATIENT MC ON STANDARD CLINICAL TESTS

Boston Diagnostic Aphasia Examination, 5178

Token Test, 2178

Peabody Picture Vocabulary Test, 7/76 (Form B)

Auditory comprehension

Word discrimination 64179 Body part identification 15120 Commands 6/S Complex material 8/12

Naming Responsive naming 16/30 Confrontation naming 88195 Animal naming 9 Body part naming 23130

Oral reading Word reading 30130 Sentence reading lO/lO

Repetition Words 9/10 High-probability sentence 118 Low-probability sentences 018

Subtests 1 II III IV v 7 3 2 2 1

Raw score = 106 Percentile = 41

z = +.5 o<z< + .5

- l.O<z< - .5 o<z< + .5

z=o .5<z<I.O z = +.5 z = +.5

z = +1.0 z > +1.0

z= +.5 z = -1.0 z = -1.0


and inferior parietal regions, with extensive involvement of the white matter in this region. This lesion is consistent with the classical and widely accepted neuroanatomical correlate of conduction aphasia (see Benson et al., 1973).

The patient lives alone, independently, and has worked occasionally as a janitor since his illness. His primary activities are reading, visiting libraries and museums, and watching television.

REPETITION TASKS

The extent and nature of MC’s repetition deficit was assessed by a set of tasks that was designed to address two broad sets of issues. First, it was necessary to establish that MC’s repetition performance was comparable to the recent case reports that have provided the data base for the interpretation of conduction aphasia as an auditory-verbal STM disorder. Second, the tasks were designed to address a number of specific issues that have assumed considerable prominence in recent discussions of conduction aphasia: (1) whether the repetition difficulties in conduction aphasia are better characterized as a “reproduction” or a true repetition deficit; (2) the effect of modality of input (auditory/visual) on the repetition deficit; and (3) whether the repetition defect is related only to memory load (list length) or is importantly affected by the type of verbal material that comprises the list or memory set.

Repetition of Digits under Different Recall Delays

The first task employed the serial recall Brown-Peterson test proce- dure, using digits as the items to be recalled. List lengths of one, two, and three digits were presented at an item rate of approximately one per second under several conditions of delay (0, 3, 6, 9, and 12 set). The digits from 1 to 9 comprised the test items. The only constraint on the composition of the lists was that no item was repeated within a list. In the conditions with delay, rehearsal was prevented by having the patient name a random series of colors as the examiner pointed to a number of colored blocks. Twenty trials of each of the delay conditions were blocked by list length, and each condition was presented once in a visual and once in an auditory mode. The results, expressed as number of correctly-repeated digit strings, are presented in Table 2.

There are three aspects of these data that should be emphasized. First, there is a major effect of mode of presentation: MC’s performance, summed over list lengths and delay conditions, shows that he could correctly repeat 200 items (67%) in the visual mode of presentation but only 117 (39%) in the auditory mode. Indeed, it appears that MC’s memory span for auditory material is reduced to one item, while it may be two items long for visual input. Second, there is a clear effect of list length, or memory load, on repetition performance: MC’s memory span


TABLE 2 NUMBER OF Dlclr LISTS REPEATED IN CORRECT ORDER

Delay (set) List

length 0 3 6 9 12

Auditory 1 19 15 13 16 13 presentation 2 8 7 8 5 6

3 3 2 2 0 0

Visual 1 20 18 16 18 19 presentation 2 19 18 14 17 12

3 11 7 3 5 3

Note. Maximum score for each condition = 20.

is at best two items long. Third, though it is not dramatic, there is some decline in correct performance with increasing delay of recall.

To examine further the locus of the repetition defect, the total number of correct items repeated was calculated independently of whether an entire string was repeated correctly. The data for the three-digit lists are presented in Table 3.

The most striking feature is the clear serial position effect (a primacy effect) in correct item recall as a function of delay. Recall of the first position item is quite good, but there is a major drop in performance for the last item; there is absolutely no indication of a recency effect.

The repetition performance of our patient parallels that of conduction aphasics described in recent reports by other investigators (e.g. Kins- bourne, 1972; Shallice & Warrington, 1977; Strub & Gardner, 1974). This type of repetition performance, when present with other symptoms, has been interpreted as consistent with a number of different theories of

TABLE 3 NUMBER OF DIGITS REPEATED WITHOUT RESPECT TO ORDER (THREE-DIGIT LISTS)

Auditory presentation

Position correct

Delay (set) Total 1 2 3

0 (37) 15-11-11 3 (33) 15-ll- 7 6 (37) 16-11-10 9 (25) 11- 7- 7

12 (25) 12- 9- 4

Note. Maximum total score for each condition = 60.

Visual presentation

Position correct

Total 1 2 3

(53) 18-16-19 (52) 19-19-14 (42) 17-14-l 1 (43) 16-15-12 (401 16-15- 9


conduction aphasia. In order to motivate more clearly the other tasks employed, we will briefly discuss the major theories of the repetition deficit in conduction aphasia by analyzing how each of these would explain the data reported thus far.

Three major classes of explanation have been offered for the repetition deficit in conduction aphasia. One type of explanation is a variant of the classical disconnection theory (Wernicke, 1874; Lichtheim, 1884; Gesch- wind, 1965; Kinsbourne, 1972). Within this argument, the repetition disorder results from a failure to transmit verbal information adequately from a short-term store to the output mechanisms. Auditory input is processed normally, and STM representations are unimpaired. Transfer of information from short-term to long-term memory (LTM), and language comprehension, are also said to be unaffected.

In Kinsbourne’s explanation of the repetition defect, the disorder “ . . . has to be attributed to a communication channel with pathologically limited capacity” (1972, p. 1131). Kinsbourne accounts for the other features of conduction aphasia by invoking a neuroanatomical explanation originally offered by Kleist (1916), in which the observed symptoms reflect the underdeveloped linguistic functioning of the right hemisphere which has been released from inhibition as a result of damage to the dominant left hemisphere.

The disconnection model has little difficulty explaining the well-known digit repetition results that we have replicated here. In the auditory input condition, the conduction aphasic can adequately process the input and store it in STM. He has difficulty when required to recall the digits, however, because information is not flowing normally from the storage buffer to the output mechanisms. The model can easily explain the decline in performance with increasing delay of recall by assuming a natural decay function in memory. One aspect of the repetition data that the disconnection model has some difficulty explaining is the superior performance obtained in the visual input condition. To account for this result, the model must assume that information from a visual store can directly communicate with the speech output mechanism. This assumption is explicitly made by Kinsbourne, but it is not clear how lexical-visual information specifies the phonemic structure of lexical items so that the speech output mechanism can be activated for repetition. In other words, at some point in the process of repetition the visual-lexical input must be translated into an auditory-verbal representation to serve as a model for the required speech response. This is an important issue that needs considerable elaboration if the model is to be taken seriously.

A second class of explanations of conduction aphasia was inspired by Goldstein’s critique of the disconnection model and his suggestion that the syndrome represents a disturbance of “inner speech”-the representation of word concepts. Goldstein’s own account of conduction


aphasia is not sufficiently specific to motivate an explanation of recent data, but Hecaen’s elaboration of Goldstein’s model has been applied to that purpose (Dubois et al., 1964; Hecaen et al., 1955; Tzortzis & Albert, 1974; Yamadori & Ikumura, 1975). The central assumption in this work is that the repetition deficit and other symptoms of conduction aphasia result from a disturbance of “the first articulation”-the mechanisms that transform an abstract acoustic mode1 or, more generally, abstract lexical representations, into the phonological forms that in turn guide the phonetic, articulatory, and graphemic mechanisms of speech output.

There are two variants of Goldstein’s general formulation that can be distinguished on the basis of where in the chain of processing the exact locus of impairment is to be situated. Dubois et al. (1964), Yamadori and Ikumura (1975), and Tzortzis and Albert (1974) locate the deficit directly at the level of encoding the phonological targets for output (henceforth, the “encoding deficit” model). Strub and Gardner (1974) argue that the deficit is at the level at which the abstract representation that guides the selection of phonological forms is constructed from a decoding of the auditory input (henceforth, the “decoding deficit” model).

As in the case of the classical model, these newer theories can account for the repetition deficit traditionally found in conduction aphasia. The encoding deficit model assumes that the patient can adequately process both visual and auditory input but that the internal representation constructed from these inputs cannot be readily encoded for output purposes because of a disruption of the output programming mechanism. It assumes further that as the input becomes more complex, the strain on the encoding device produces not only errors of omission and paraphasias, but also ordering problems in which the elements of a string are encoded in the wrong order. This model explicitly addresses an aphasic symptom that is assumed to be an important component of conduction aphasia: phonemic paraphasias. It completely fails, however, to provide an explanation of the superior repetition of words presented visually.

The decoding deficit mode1 argues that the repetition deficit in conduction aphasia is the result of reduced efficiency in decoding speech, which places various levels in the decoding process in competition for limited processing space. This model has the advantage of being able to explain subtle comprehension deficits that can be found in conduction patients. As in the case of the encoding deficit model, however, it fails to offer a motivated account for the disparity in repetition performance for the visual and auditory input conditions.

The most thoroughly developed mode1 of the repetition disorder found in conduction aphasia is the auditory-verbal STM deficit mode1 proposed by Warrington and Shallice (1969). This mode1 assumes that the repetition


deficit is not secondary to a disturbance of specifically linguistic mechanisms. Rather, the impairment is a reduction of auditory-verbal STM capacity to a memory span that is much reduced from the normal storage capacity of approximately seven units of information (Miller, 1956).

This model can account for repetition performance in the auditory condition; more importantly, the superior performance for the visual input condition can be explained by assuming that a visual STM store is functioning normally. This model can also handle quite naturally a number of interesting aspects of the repetition data and other types of memory performance. For example, it correctly predicts that conduction aphasics should be able to make effective use of long-term memory in repetition tasks because semantic information can be entered directly into LTM without the necessity of short-term storage. Finally, this model assumes that aphasic symptoms associated with conduction aphasia are secondary to the STM deficit. For example, the comprehension difficulties found in these patients reflect the inadequate support of a working memory system during sentence parsing and interpretation. These issues will be discussed further below.

Now that we have presented the three classes of models that have been proposed to account for the repetition disorder in conduction aphasia, we can evaluate each of them by considering our patient’s performance on several repetition and recognition tasks.

Single-Item Probe (Recognition Task)

This task was designed to assess MC’s STM without requiring him to retain serial list information or to repeat the items in the list. A memory probe technique was used that was similar to that employed by Shallice and Warrington (1970). A four-item list was read, followed by a single- probe item, and the patient was to say whether the probe item had been part of the list. One hundred sixty lists of concrete nouns were prepared and the probe item was part of the list on half the trials. The patient’s task was to decide whether the probe item was contained in the list he had just heard. The number of correct responses for each serial position probed (out of a possible 20 correct) is shown in Table 4.

The overall rate of performance (74% correct) was comparable to the

TABLE 4 NUMBER OF CORRECT RESPONSES TO SINGLE ITEM PROBE FOR EACH SERIAL POSITION

Number correct

1

17

Serial position 2 3 4

11 14 17

Note. Maximum score for each position = 20.


performance of Warrington and Shallice’s patient KF (76% correct). Importantly, there appears to be a serial position effect for both primacy and recency items. What should be emphasized about these results is that, although MC’s performance here is superior to his performance in recall tasks (see next experiment), it is nonetheless markedly impaired. This suggests that, for MC as well as for KF, the STM representation for a four-item list is not normal.

The results of this experiment are consistent neither with the disconnection model nor with the encoding deficit explanation of the repetition deficit. Both of these assume that the input is processed adequately and that a normal internal representation of the input string is constructed. The decoding deficit model and the auditory-verbal STM model can easily accommodate the results of this experiment because both predict that the internal representation of the input string should not be normal.

The first two experiments have established that MC has a profound repetition deficit that cannot be explained as a disconnection or as an encoding disorder. MC’s performance on the repetition task is qualita- tively identical to the cases reported by Warrington and Shallice (1969), Saffran and Marin (1973, Tzortzis and Albert (1974), Strub and Gardner (1974), and Kinsbourne (1972). Interestingly however, Kinsbourne’s two cases had a remarkable list recognition ability that contrasted sharply with their repetition performance. The recognition ability of these patients presents a striking contrast to the performance of Warrington and Shallice’s patient and to that of MC. This discrepancy will be considered further in the Discussion.

Repetition of High-Frequency Nouns, Low-Frequency Nouns and Function Words

One of the characteristics of repetition performance that Warrington and Shallice have interpreted as support for the STM disorder hypothesis is that their patient’s ability to repeat items appears to be related to the length of the list rather than to the types of items in the list. This argument is at variance with the widely reported clinical observation that conduction aphasics have considerably more difficulty repeating the grammatical function words-articles, auxiliaries, conjunctions, etc.-than repeating nouns (e.g. Goodglass 8z Kaplan, 1972). If this clinical observation is correct, it could be a source of difficulty for the STM hypothesis, as well as for the decoding deficit hypothesis. In this experiment, we tried to quantify the reported clinical impression of a differential repetition impairment as a function of list material.

Three types of words were used: high-frequency concrete nouns, low- frequency concrete nouns, and function words. The two noun sets contained an equal number of one-, two-, and three-syllable words. The experimental paradigm used was the Brown-Peterson serial recall pro-


cedure with 0- and 9-set delays. List lengths were one, two, three, and four words presented at a rate of approximately one item per second in 25-list blocks. There were separate auditory and visual presentation conditions. Results for this task (number of correct lists recalled) are shown in Table 5.

Three aspects of these data should be emphasized. First, as in Ex- periment 1, there is a marked effect of mode of presentation, with the visual condition superior to the auditory condition. Second, there is a slight effect of frequency, with high-frequency nouns recalled better than low-frequency nouns in the visual presentation condition. Third, and most important. is the difference in the patient’s ability to recall function words relative to nouns in the two modes of presentation. MC had serious difficulty recalling even a single function word when these words were presented aurally; when they were presented visually he could recall them as well as nouns in both the immediate and the delay conditions.

To obtain a more precise assessment of MC’s repetition performance, we analyzed item recall independently of serial recall performance. These data (in the form of percentage of total items correct without regard to whether they were recalled in the correct order) are presented in Tables 6 (three-word lists) and 7 (four-word lists). The data are averaged over delay conditions, where relevant, as no appreciable differences were obtained as a function of delay. These data replicate in part the results obtained in Experiment 1. More importantly, they show an effect of word frequency that is considerably stronger in the visual than in the auditory presentation condition. A further aspect of these data to be emphasized is the very small number of function words recalled in the auditory condition: 15 and 7% for the three- and four-item lists, respectively.

The data from this experiment were reanalyzed to address the issue of whether item repetition performance was a function of the number of syllables in the words to be repeated. A number of investigators have reported that some conduction aphasics have more difficulty repeating long than short words (Dubois, et al., 1964; Yamadori & Ikumura, 1975). This form of deficit (termed a “reproduction” disorder) is necessarily predicted by both the disconnection and the encoding deficit models, although it is not inconsistent with any of the hypotheses that have been offered. Shallice and Warrington (1977) have suggested that a reproduction problem may reflect a different type of disorder than the classic repetition deficit and that we should treat patients with these two types of symptoms separately. To determine whether MC’s repetition difficulties were primarily a reproduction disturbance, we analyzed repetition of high-frequency nouns in the auditory presentation condition as a function of syllable length. Table 8 presents these data for words of one, two, and three syllables in the form of proportion of correct items recalled. It is immediately clear that there were no appreciable differences

TABL

E 5

NUMB

ER

OF

LIST

S RE

PEAT

ED

IN

CORR

ECT O

RDER

(CON

CRET

E NO

UNS

AND

FUNC

TION

W

ORDS

)

No

dela

y D

elay

(9

set

)

List

Li

st

leng

th

Hi-f

req.

Lo

w-fr

eq.

leng

th

Hi-f

req.

Lo

w-fr

eq.

P (w

ords

) no

uns

noun

s Fu

ncto

rs

(wor

ds)

noun

s no

uns

Func

tors

$

Audi

tory

I

22

21

13

1 24

24

12

$

pres

enta

tion

2 11

14

1

2 14

13

0

3 1

1 0

3 2

0 NT

F

4 1

0 0

4 1

NT

NT

2

Visu

al

1 25

25

24

1

25

23

24

F pr

esen

tatio

n 2

25

25

20

2 21

16

18

3

13

5 I

3 4

1 7

4 I

0 0

4 2

0 0

No&

. M

axim

um

scor

e fo

r ea

ch c

ondi

tion

= 25

. ”

Patie

nt

was

nor

reste

d on

a c

ondi

tion

if he

fai

led

to p

rodu

ce

at l

east

one

cor

rect

re

petit

ion

of t

he p

rece

ding

lis

t.


TABLE 6 PERCENTAGE OF WORDS REPEATED CORRECTLY WITHOUT RESPECT TO CORRECT ORDER

(THREE-WORD LISTS)

Auditory presentation Frequency

High Low

Mean percentage correct

Visual presentation Frequency

High Low


Auditory presentation Visual presentation

Total percentage correct

Nouns

49 78 38 30 49 78 38 32

49 78 38 31

71 72 64 78 53 78 52 30

62 75 58 54

Function words I5 60

Percentage serial position correct

32 8 4 72 58 50

3

in repetition as a function of syllable length. This result strongly suggests that MC’s difficulties in repetition should not be characterized as a disorder of reproduction.

Several aspects of the results of this experiment are inconsistent with the disconnection, the encoding and the decoding deficit hypotheses. None of these models can explain the superior performance for visually presented lists or the fact that function words were very poorly repeated in the auditory, but not in the visual, condition.

The STM deficit hypothesis successfully predicts the advantage of visual input, but appears to have some difficulty explaining other aspects of these results. First is the observation that a frequency effect was obtained in the visual rather than in the auditory condition. Warrington and Shallice have argued that recall in the auditory input task consists primarily of information from LTM, whereas recall in the visual input task is from an undamaged visual STM in addition to LTM. By this reasoning, it is expected that the frequency effect (which reflects information coming from LTM) should be most strongly manifested in the auditory mode condition. However, our results showed the opposite effect: a greater effect of frequency in the visual condition.


TABLE 7 PERCENTAGE OF WORDS REPEATED CORRECTLY WITHOUT RESPECT TO CORRECT ORDER

(FOUR-WORD LISTS)

Percentage serial position correct

Total percentage correct 1 2 3 4

Auditory presentation Frequency

High Low


Visual presentation Frequency

High Low


Auditory presentation Visual presentation

Nouns

42 76 48 20 24 32 76 32 4 16

39 76 43 I5 21

63 70 66 44 72 39 68 28 24 34

50 69 47 34 53

Function words 7 12 8

37 68 46 4 4

24 8

Perhaps a more disturbing result is the effect of presentation mode (visual vs. auditory) on the patient’s repetition of function words relative to nouns. MC’s ability to repeat function words when presented aurally is severely limited. This limitation cannot be attributed to an ordering output problem (Tzortzis & Albert, 1974), since MC had difficulty repeating even single-word lists of function words (see Table 5). It appears

TABLE 8 PROPORTION OF THREE-, Two-, AND ONE-SYLLABLE HIGH-FREQUENCY NOUNS REPEATED

CORRECTLY (AUDITORY PRESENTATION, ~-SEC DELAY)

List length (words)

Number of syllables

3 2 1

1 2 3 4

Mean proportion correct

1.0 I.0 1.0 1.0 .88 .88 .50 .56 .72 .85 .48 .38

.78 .63 .65


that the form of the representation that MC can construct for aurally presented words is particularly impoverished for function words.

Warrington and Shallice have argued that “a reduction in all auditory verbal span tasks, performance being related to the ‘string’ length rather than the characteristics of individual speech sounds, is prima facie evidence of an impairment of the short term memory store” (Warrington et al., 1971, p. 385). Since our patient’s repetition performance was significantly affected by the type of stimulus material presented, we must consider whether the STM hypothesis can be interpreted to accommodate this result. For example, it might be argued that, unlike nouns, function words lack clear (nonsyntactic) meaning when presented without a sentence context and that they are, therefore, not processed as fully as nouns. Under such circumstances, the LTM representation for function words is not developed or is developed poorly. The lack of a well- developed LTM representation would force the patient to recall function words strictly from STM, which is impaired, thus leading to the severely impoverished repetition performance. This is not an implausible line of reasoning, and it leads to a testable prediction: when function words are used in the normal syntactic role they should receive adequate “semantic” analysis to produce a strong LTM representation. That is, recall of function words should improve when they are embedded in phrasal contexts.

Repetition of Phrases

To test this prediction, we asked MC to repeat ten function word/noun phrases. Each phrase was read slowly but with normal intonation. As shown in Table 9, MC repeated correctly all ten nouns, but only one function word. He was fully aware that two words were presented on each trial, and he even seemed aware of the fact that the first word was

TABLE 9 REPETITION OF FUNCTION WORD/NOUN PHRASES

Stimulus item

Patients’ responses

The gun in bed a dog

among friends between cars at home few people under blankets up ladders some flowers

-gun in bed --dog (“dog . . . dog something dog”) on friends beneath cars on home -people “und” blankets on ladders on flowers


a function word. The incorrect function words he produced were artic- ulated normally. It should be emphasized here that MC’s problem with function words is a repetition-induced pathological behavior; in conver- sational speech and writing he uses function words in a relatively normal way.

The assumption motivating this experiment was that function words used in a syntactic context would receive semantic processing that would result in an adequate LTM trace that could be used to aid repetition. It is possible that the manipulation employed here (isolated two-word phrases) did not in fact lead to a more effective semantic analysis of function words. Alternatively, it may be that function words do not in general receive a semantic analysis and that there is no condition in which repetition of function words could rely on an LTM component. If either of these alternatives is true, this experiment was not a fair test of the STM-deficit hypothesis.

Finally, it should be noted again that the results obtained in this and in the previous experiment are not consistent with any of the hypotheses that have been offered to explain conduction aphasia. That is, predictions about differential repetition performance as a function of form class distinctions do not follow naturally from any of these hypotheses as they were originally formulated.

Repetition of Nouns with h4anipulations of Delay

The last experiment in this section was designed to assess the effects of two other presentation parameters on repetition performance to allow further distinctions among the four hypotheses concerning the nature of conduction aphasia. One question was whether allowing the patient to rehearse the input (unfilled delay condition) would improve his performance relative to performance in a condition in which rehearsal was blocked by an extraneous task (filled delay). The other issue explored was the effect of rate of presentation on the patient’s repetition. If impaired repetition is based on the patient’s inability to encode the items for output (encoding deficit hypothesis), these input manipulations should have little effect on performance.

Three conditions were employed, all using 25 three-word lists com- posed of high-frequency nouns. In one condition the patient was presented aurally with the three-word lists at a rate of one item per second and a filled, 9-set delay preceded recall of the list. The distractor task was, as in previous cases, the rapid naming of colored blocks. The second condition was identical to the first except that no distractor task was interspersed between the presentation of the list and the point of recall. That is, the patient was allowed to rehearse the list for 9 set prior to recall. In the third condition, items were presented at the rate of one


every 3 set, and an unfilled delay of 3 set was introduced between the third item and the point of recall. Thus, the time between the presentation of the first item and recall was about equal for the three experimental conditions, but the potential for rehearsal was varied.

Table 10 presents the number of serially correct lists recalled, the total number of items recalled, and the number of items recalled for each serial position for the three conditions. The total number of words recalled is about equal for each condition. However, there are clear interactions of delay condition by number of serially correct lists recalled, and of delay condition by serial position of items recalled. From these results it appears that the major effect of preventing rehearsal is on serial recall performance, whereas rate of presentation most clearly affects the serial position of items recalled.

The results of this experiment present insurmountable difficulties for the encoding deficit hypothesis. This model assumes that the locus of the disorder is in the encoding of a relatively well-constructed and well- preserved internal representation into a phonological string for output. However, as a comparison of the filled and unfilled delay conditions indicates, serial recall performance is a function of differential forgetting of order information from STM due to the prevention of rehearsal. Fur- thermore, the encoding deficit hypothesis fails to provide a motivated account for the recall of items from different serial positions in the unfilled delay condition and the slow rate of presentation condition. Consideration of these two tasks suggests that item recall as a function of serial position is determined by some input variable that affects the form of the internal representation and is apparently unrelated to any hypothesized disruption of the encoding mechanism. It should be emphasized that these differences in serial position performance occur in

TABLE 10 NUMBER OF HIGH-FREQUENCY NOUNS RECALLED AS A FUNCTION OF THREE DELAY

CONDITIONS (THREE-WORD LISTS)

Serial position

Seriallv correct Total words correct

Delay condition lists correct 1 2 3

9 set, with distractor 2 46 22 14 IO

9 set, no distractor 8 48 21 17 10

3 set, between items 8 51 16 17 18

Note. total number of lists for each delay condition = 25


the context of equal performance in serial recall and total item recall. This pattern of performance cannot be explained by assuming a disruption at the level of the encoding of output.

The disconnection hypothesis has comparable difficulty accounting for the pattern of results we have reported. That is, this hypothesis also fails to predict the interactions for the two comparisons we have made above.

Both the STM and the decoding deficit hypotheses are successful in accounting for one of the interactions between conditions, but both fail to account for the other comparison. In order to discuss the predictions made by the STM hypothesis we need consider in more detail Shallice and Warrington’s model (1970). This model assumes that there are par- allel inputs into STM and LTM, as well as a “rehearsal loop” that provides a means for keeping information “active” in STM. Shallice and Warrington argue that the repetition deficit results from a pathological limitation of the short-term store, but this limitation should not prevent the “normal” functioning of the rehearsal circuit. The fact that rehearsal is possible, though perhaps with reduced efficiency, allows the generation of fairly normal LTM representations of lists that do not exceed the capacity of the impaired short-term store in conditions that allow for rehearsal. One prediction that follows from this is that there should be a different pattern of serial position recall as a function of rate of presentation. In the condition with delay between items, the patient can presumably rehearse each word sufficiently to achieve an adequate LTM representation. When items are presented more rapidly, the patient cannot make efficient use of the rehearsal system and the later items on the list are processed inadequately for LTM storage.

A similar prediction, based on different principles, is made by the decoding deficit hypothesis. This model assumes that in the slow presentation condition each item can be processed adequately; in contrast, in the rapid presentation condition the inefficient decoding system cannot process to a sufficient extent the later items in the list. Thus, both hypotheses successfully predict a different pattern of serial position results for the rate of presentation contrast.

Although these two hypotheses correctly predict a difference in serially correct performance for filled and unfilled delay conditions, they en- counter difficulties with the serial position data. Specifically, both of these hypotheses predict a recency effect for the unfilled delay condition. In the case of the STM hypothesis, a recency effect is predicted by the assumption that the rehearsal system is normal and thus the last item should receive normal rehearsal. The decoding deficit hypothesis similarly assumes that the last item before the unfilled delay should receive “deeper” processing than the last item in the filled delay condition since there is no interfering process to block the “deeper” processing needed for good recall.


Both hypotheses can account for the major portion of these results, but neither explains the entire pattern.

DISCUSSION OF REPETITION TASK RESULTS

There are four major features that characterize MC’s repetition abilities in the tasks we have presented to him. Two of these features have also characterized the recent cases of conduction aphasia reported in the literature-severely restricted memory span and superior repetition of visually relative to aurally presented material. A third aspect of MC’s repetition performance distinguishes our case from some of the other cases reported. Specifically, MC has no deficit in the fluency of his speech; he could repeat three-syllable words about as well as he could repeat monosyllables (see Table 8). In this respect he is similar to cases KF and JB reported by Warrington and Shallice, and case IL reported by Saffran and Marin. All of these cases clearly differ, however, from the cases reported by Kinsbourne, by Dubois et al., and by Yamadori and Ikumura, all of whom were described as having considerable difficulties in the “reproduction” of presented targets. Finally, MC presented an exaggerated deficit in repetition of aurally presented function words in comparison to nouns, but no differential effect of form class when the items were presented visually. Although this particular pattern of deficits involving form class distinctions has not previously been reported in case studies of conduction aphasia, it is not unexpected when we consider the clinical descriptions of that disorder (e.g. Goodglass & Kaplan, 1972).

Shallice and Warrington (1970) have made an attempt to distinguish between subgroups of patients having difficulty with repetition: one group can be said to have a disorder of “reproduction,” and they have particular difficulty with multisyllabic words; the other subgroup is characterized by a “pure” repetition deficit that is less affected by the number of syllables in the words that are to be repeated (See also Luria, 1976). This distinction is heuristically valuable in that it provides the opportunity for formulating theories of cognitive disorders for relatively homogeneous populations of patients. Shallice and Warrington argue that the classification “conduction aphasia” should be restricted to those patients whose spontaneous and imitative speech output is clearly paraphasic, and whose repetition difficulties are based on a deficit of speech reproduction. Patients who have comparable difficulty repeating long and short words, and whose spontaneous and imitative speech is not paraphasic, should be classified as patients with an STM deficit, rather than as conduction aphasics.

We agree with Shallice and Warrington that the patients who have been described as conduction aphasics do not constitute a homogeneous group. It is clear that the two cases reported by Kinsbourne, for example, are different from our case and from the cases reported by Warrington


and Shallice. From the clinical description that Kinsbourne presents, his patients appear to have lesions in the anterior language regions, whereas our case presents the classically established parietal-temporal involvement. In addition, Kinsbourne’s two cases had the remarkable ability to discriminate identical pairs of eight item lists from nonidentical pairs- an ability that appears to rule out an STM impairment. MC’s performance is significantly inferior, as he achieved only a 75% level of accuracy in a single item probe of a four-word string (see also Shallice & Warrington, 1970). The patients described by Tzortzis and Albert and by Yamadori and Ikumura also appeared to have difficulties with the reproduction of speech. Indeed, a major factor underlying the formulation of the encoding deficit hypothesis was the presence of literal paraphasias in their patients’ speech.

It must be noted that the distinction drawn here is not an easy one to make-MC, as well as Strub and Gardner’s patient LS, produced occasional paraphasias in spontaneous speech. Nonetheless, the neuroanatomical and behavior discrepancies apparent in the recent case reports strongly support Shallice and Warrington’s efforts to narrow discussion to more homogeneous cases.

Considering the distinctions drawn above, it would appear that MC’s performance should be classified as a relatively pure repetition disorder. The experimental results presented here indicate that the source of MC’s impairment cannot be attributed to the classically defined disconnection of the language areas, nor is it possible to attribute it to a disorder of the “first articulation” as defined by Dubois et al. (1964) and further developed by Tzortzis and Albert (1974) and Yamadori and Ikumura (1975). Rather, it appears that MC’s repetition defect is based on a disruption of the memory trace that serves as a model for repetition. The evidence for this assessment consists of the following features of MC’s performance. First, the results of the memory probe task clearly indicate that his memory representation for a four-item list is seriously impaired. Second, the experimental parameters that affected MC’s repetition performance (e.g., rate of presentation, the prevention of rehearsal during delay, etc.) were primarily factors that determine the form of the internal representation that is constructed upon the presentation of the to-be- repeated material. Third, differences in repetition performance as a function of mode of input suggest a specifically auditory storage deficit. Fourth, the differential effect of form class on repetition indicates that an inadequate representation is constructed for function words when they are presented aurally.

Although the results suggest that our patient’s disorder should be considered as occurring at the level of memory representation, the precise nature of this disorder is far from clear. Specifically, such a disorder could result from several sources, including the pathological limitation


of capacity in the short-term store suggested by Warrington and Shallice, or the decoding deficit offered by Strub and Gardner.

The first two of the results summarized above can be accommodated equally well by the decoding deficit hypothesis and by the STM-deficit hypothesis. The third finding-superior repetition of visually presented material-is naturally predicted by the STM deficit hypothesis but not by the decoding deficit view. Strub and Gardner have argued that there may be an alternative route for processing visual information, but this “explanation” is not motivated by any independent considerations. If this account is accepted, however, it implies that visual processing in all tasks should be superior to auditory processing. This is an important point to which we shall return.

The fourth result-disproportionately impaired repetition of aurally presented function words-is not easily accommodated by either the STM deficit or the decoding deficit hypothesis. We have suggested that the representation of function words is particularly affected in the case of disordered memory representation because these words have little semantic information to supplement the short-term representation that is presumably coded phonologically. Although these arguments can rea- sonably be made, they considerably expand both hypotheses as they were originally formulated.

At this point we may want to reassess whether a unitary deficit hypothesis can account for the observed pattern of deficits in even a single conduction patient. This need for a reassessment becomes even more pressing if we broaden the scope of our explanatory theories to include aphasic symptoms in addition to the repetition defect. Thus, for example, how do the decoding and the STM deficit hypotheses account for the very poor performance of our patient, the patient of Strub and Gardner, and those of Warrington and Shallice on the Token Test? How is the STM deficit in Shallice and Warrington’s case KF related to that patient’s reported reading disorder (Shallice & Warrington, 1975)? Does the fact that our subject does not share KF’s reading deficit have any bearing on the issue of whether a similar disorder characterizes these two cases?

In order to characterize fully a patient’s disorder, it is of paramount importance to analyze his performance not only on the major symptom of interest but also on related behaviors. Broadening the focus beyond the most readily apparent deficit serves two important functions: first, it helps distinguish among the cases that are taken to be clear instances of a syndrome; and second, a careful analysis of the patterns of cooc- currences of symptoms should importantly constrain the development of theories of aphasia. By assessing patients’ abilities on a wide range of tasks, we may avoid the real danger of selecting the symptoms to fit, rather than to inform, our theories.


LANGUAGE TASKS

In an effort to provide a comprehensive picture of our patients’ aphasic symptoms, we tested MC’s language performance in four areas: oral reading, speech production, sentence comprehension (auditory and visual), and sentence construction (anagram). These particular language functions were tested in order to obtain information comparable to that available on some of the other reported cases of “conduction aphasia” (e.g., KF on oral reading); to explore more fully MC’s difficulties with function words; and to obtain a relatively precise assessment of MC’s language processing capacities.

Oral Reading

In their comprehensive review of studies on conduction aphasia, Green and Howes (1977) report that the majority of conduction patients present moderate reading impairments. The overall ratings that they report do not reveal the nature of the reading difficulties exhibited by the patients, and few of the case studies reported describe the reading disorders of conduction aphasics. Thus, we have no knowledge of whether these patients were “deep dyslexics,” as was case KF reported by Shallice and Warrington (1975), or whether the patients’ reading difficulties were primarily at the level of visual confusions or “literal” paralexias that might be related to an output encoding disorder.

MC was presented with 205 single words and 39 sentences which he was asked to read aloud. The single words consisted of high- and low- frequency concrete nouns, abstract nouns, verbs, adjectives, function words, nonword pseudo-homophones (e.g. “bate”), and pronounceable letter strings (e.g., “bewlet”). The sentences contained both abstract and concrete nouns and included indirect object constructions, prepo- sitional phrases, WH questions, imperatives, passives, and subordinate clause constructions.

Single words and sentences were typed on cards and the patient was given as much time as he needed to read the words aloud. MC’s oral reading of the single words is presented in Table 11 in the form of percentage correct. This table also shows data obtained from a patient classified as a Broca’s aphasic, who was tested for comparison purposes. A Broca patient was chosen because of MC’s special difficulties in repeating function words. It is well known that Broca’s aphasics have particular problems processing function words (Caramazza & Berndt, 1978), and it is important to compare those problems with the difficulties that conduction aphasics experience with that class of words.’

’ A mildly impaired Wemicke’s aphasic was also tested on all tasks reported here. This patient was included to assure that the syntactic disturbances that are of interest cannot be said to occur as a general feature of aphasia. The Wemicke patient showed no evidence of syntactic processing difficulties, nor selective disruption of function words relative to other classes of words.


TABLE 11 PERCENTAGE OF WORDS READ CORRECTLY IN EACH FORM CLASS

Nouns High-frequency,

concrete (N= 23) Low-frequency,

concrete (N = 23) Abstract

Verbs (N= 20)

Adjectives (N = 20)

Function words (n = 20)

Nonwords Pseudo-homophones

(N= 10) Pronounceable

strings (N = 20)

Patient MC Broca Patient

100 96

96 70

86 43

95 75

95 65

95 20

50 10

60 5

An inspection of this table reveals that MC had no serious reading problems, at least for real words. His overall performance with real words is 95% correct. The few errors that occurred were literal paralexias. He had more trouble reading nonwords, and seemed poorly dis- posed to attempting these “strange” items. In contrast to MC, the Broca’s aphasic had a lower level of performance overall for every cat- egory tested, and also displayed marked difficulty reading function words, abstract words, and nonwords. Indeed, this patient’s pattern of performance is similar to KF, the deep dyslexic case reported by Shallice and Warrington.

MC’s reading of sentences was also excellent. He made only 7 errors in 39 sentences and these were local and relatively insignificant. For example, he read “what is your near idea” instead of “what is your new idea.” In general, MC had no difficulty reading function words. In contrast, the Broca’s aphasic did not read a single sentence correctly and, as expected, had considerably more difficulty reading the sentences with abstract nouns and those with a preponderance of function words.

From these results it appears that MC can process visually presented words sufficiently well to assign them a correct phonological representation and can then use this representation to determine the articulatory form necessary for the proper production of the word.

Although MC has difficulty repeating aurally presented function words he has no special trouble reading words of this type. The Broca patient, on the other hand, was severely impaired in his ability to read function words.


Sentence Production (Story Completion Task)

We have emphasized that MC’s spontaneous speech production is relatively normal. To quantify that clinical impression, we elicited speech samples using the Story Completion Test (Goodglass, Gleason, Bern- holtz, & Hyde, 1972). This test involves the presentation of a two- or three-sentence “story” which leads to a sentence fragment that the patient is required to complete. For example, when presented with the sequence: “the grass needs to be cut. I give my son the lawn mower and I tell him . . .,” the patient is expected to complete the sentence with an imperative construction. There are 28 items designed to elicit 14 different types of syntactic frames. The test was administered to MC twice, once aurally and once visually. The Broca patient was given only the auditory version of the task.

Results of this task are presented in Table 12. In the auditory version of the test, MC produced four inappropriate responses and one “no response,” while more than half of the Broca patient’s responses were inappropriate. If responses are assessed strictly in terms of whether they are agrammatic, MC produced only two deviant responses, while considerably more of the Broca patient’s responses were agrammatic. Fi- nally, although MC’s responses were for the most part appropriate in terms of context, they were often not given in the form elicited by the story fragment.

MC’s performance on the visual version of the test was somewhat worse than his performance on the auditory version in that he produced a larger number of inappropriate responses (indicating poorer comprehension of the visually presented material). The actual form of his re-

TABLE 12 NUMBER AND ANALYSIS OF COMPLETIONS SUPPLIED IN STORY COMPLETION TASK

Patient MC Broca Patient

Classification of Standard Visual Standard patient’s response administration administration administration

Correct completions 11 9 1 Appropriate response,

but not target 10 5 5 constructions

Completion inappropriate, but 4 12 11 not agrammatic

Completion agrammatic 2 - 11

No response 1 2 -

Note: Total items = 28.


sponses, when assessed for the proper use of function words and grammatical well-formedness, did not differ appreciably from the level of performance in the auditory version of the test.

The results obtained in this task reveal that MC has considerable mastery of the use of function words, although his comprehension of the “story” fragment is somewhat disturbed. In particular, it appears that MC gets the general gist of the story fragment without fully processing the syntactic form of the sentences that he is expected to complete. The Broca patient’s comprehension performance represents an essentially more severe form of MC’s deficit.

Comprehension of Sentences

As we have indicated, MC’s language comprehension, although near normal on clinical testing, is quite impaired when assessed more rigorously. His performance on the story completion task suggests poor syntactic comprehension in both visual and auditory modalities. Similarly, MC’s comprehension on the Token Test (DeRenzi & Vignolo, 1962) was significantly impaired in both modalities. The presence of poor comprehension in conduction aphasia is more prevalent than would be assumed from the clinical description. Warrington and Shallice and Strub and Gardner report that their patients have severe comprehension difficulties when assessed by the Token Test. Furthermore, Green and Howes (1977) report that most of the conduction cases reviewed in the literature have impaired comprehension. Of the 37 cases reported in which comprehension performance was tested in both modalities, 25 are described as having mild to moderate auditory comprehension impairments, with visual comprehension significantly poorer. A comparison of comprehension in individual cases reveals that 22 of 37 patients were more impaired in the visual than in the auditory modality, 11 showed an equal impairment and 4 showed a reversal.

Two recently published studies report that conduction aphasics produced a pattern of comprehension deficit that was identical to that of Broca’s aphasics (Caramazza & Zurif, 1976; Heilman & Scholes, 1976). For example, Caramazza and Zurif showed that conduction and Broca’s aphasics (as a group) had good comprehension of sentences in which the meaning could be uniquely determined by comprehension of the major lexical items without regard to syntactic relations (e.g., “the apple that the boy is eating is juicy”). Both patient groups performed at chance level with semantically reversible sentences, that is, sentences in which an appreciation of the syntactic relations among major lexical items is necessary for the assignment of a semantic interpretation (e.g., “the boy that the girl is chasing is tall”).

One other indication of the nature of the comprehension deficit can be inferred from a case report by Saffran and Marin (1975), who asked


their patient to repeat semantically constrained or semantically reversible sentences. When attempting to repeat, their patient often produced accurate paraphrases of semantically constrained sentences, but tended to reverse the meaning when repeating semantically reversible (passive) sentences. This result suggests that the patient did not recover the proper syntactic structure for the semantically reversible sentences and assigned them incorrect meanings.

The studies by Caramazza and Zuriff, Heilman and &holes, and Saf- fran and Marin suggest that the comprehension deficit in conduction aphasia can be characterized as resulting from an inability to process or to represent syntactic information adequately. This hypothesis was tested with respect to MC’s comprehension impairment.

A sentence-picture matching task was used. Of 72 items, 36 sentences were semantically reversible (e.g. “the cat is being chased by the dog”) and 36 were semantically constrained (e.g. “the bone is being eaten by the dog”). Several syntactic forms were included: actives, passives, and subject-relative and object-relative subordinate clause constructions. The sentences were presented to the patient twice, once visually and once aurally. In the visual presentation condition, the patient was given as much time as he needed to study the sentence before choosing one of four pictures. Similarly, in the auditory presentation condition the patient was given as many repetitions of the sentence as he wanted before he decided to respond. The pictures were not in front of the patient while he was reading or hearing the sentences; thus, he could not systematically eliminate inappropriate pictures using partial information. The four pictures presented with each sentence consisted of a correct depiction of the sentence; one picture that differed from the correct one in that different objects from those described in the sentence participated in the action described by the verb (lexical distractor); one picture (for the reversible sentences only) that reversed the relation between the two objects named in the sentence (the syntactic distractor); and one picture (or two in the semantically constrained sentences) that differed in both objects and actions from the target picture (lexical distracters).

The number of correct responses and the distribution of error types are shown in Table 13. Overall, MC’s performance was slightly better than that of the Broca patient. Of particular interest is the comparison of performance on the semantically constrained and the semantically reversible sentences for the two patients. Both performed worse on the reversible sentences than on the semantically constrained sentences. More importantly, an analysis of error types shows that both MC and the Broca patient made substantially more “syntactic” than lexical errors in the visual presentation condition.

Two aspects of these results should be emphasized. First, the pattern of comprehension for the conduction aphasic is remarkably similar to


TABLE 13 ANALYSIS OF RESPONSES-SENTENCE COMPREHENSION TASK

Sentence type Presentation

mode Total correct

Error type

Lexical Syntactic

Nonreversible

Reversible

Visual Auditory

Visual Auditory

Nonreversible

Reversible

Visual Auditory

Visual Auditory

Patient MC 32 29

21 16

Broca patient 22 27

17 16

4 - 7 -

2 13 9 11

14 - 9 -

2 17 10 10

Note: Maximum number correct in each condition = 36.

that of the Broca patient in that both made more syntactic than lexical errors in the reversible sentences. This result supports Caramazza and Zurif’s (1976) suggestion that conduction aphasics may have asyntactic comprehension. Second, there is a marked interaction of error type by input modality for both patients. This result shows that neither patient could adequately recover the syntactic structure of sentences even when given unlimited time to process the sentences.

Sentence Construction (Anagram) Task

Thus far we have found that MC has asyntactic comprehension like a Broca patient, but that, unlike the Broca’s aphasic, he is not agrammatic in the production of sentences or in oral reading. To investigate further this intriguing dissociation of syntactic processes we tested MC and the Broca control on an anagram task. All the lexical information, including syntactically relevant cues such as function words and bound grammatical morphemes, is given to the patient. His task is to rearrange the words to produce a meaningful sentence. It is assumed that in this sit- uation the performance of the patient reflects fairly directly his grammatical knowledge of the language (von Stockert & Bader, 1976; Kremin & Goldblum, 1975). There are no output constraints such as articulatory and encoding difficulties, or word finding problems to mask the patient’s knowledge of the syntactic and semantic organization of a sentence.

The 15 sentences used in this task were varied in syntactic form from simple active, affirmative sentences to questions, passives, and indirect object constructions. Each word of a sentence was printed on a separate card and the cards were presented to the patient in a scrambled order.


The patient was given as much time as he needed to rearrange the cards into a meaningful sentence. The results of this experiment provide a striking contrast in performance between the two patients. MC rear- ranged all 15 scrambled sentences to produce correct responses. He was provided with cues (next word in the string) in only two sentences. In all other instances he had no major difficulty successfully completing the task, but he performed quite slowly and carried out the task with what appeared to be a trial-and-error strategy. In contrast, the Broca patient failed to rearrange 6 of 15 sentences, despite considerable cueing. The patient was able to rearrange only two of the sentences without assist- ance. It was clear that the Broca’s aphasic did not appreciate the syntactic function of grammatical morphemes. Examples of the two patients’ attempts to rearrange a scrambled sentence are presented in Table 14. One striking aspect of the Broca patient’s,behavior was that he appeared to be totally insensitive to the grammatical violations in the strings. he produced. Unlike the Broca’s aphasic, MC was quite aware of the syntactic role of function words, although he appeared to use a trial-and- error strategy in solving the task.

The results of this experiment offer another example of the differences in language processing abilities between the conduction and the Broca’s aphasics. While the Broca patient does not seem to have access to syntactic information in any of the language functions tested, the conduction aphasic can, under appropriate circumstances, gain access to syntactic knowledge to guide his language performance.

DISCUSSION OF LANGUAGE TASKS

MC’s performance on these four language tasks reveals an interesting pattern: “normal” performance in oral reading, speech production, and

TABLE 14 SAMPLE RESPONSES-SENTENCE CONSTRUCTION (ANAGRAM) TASK

Target sentence: “The boy gave it to the dog.”

Patient MC the boy gave the dog gave it the boy gave it to the dog

Broca patient boy gave dog

the to the it the boy gave dog

to the it the it boy gave dog

to the the it boy gave the to dog the boy gave the dog to it

Comments moves slowly rejects; says “no” correct

substantives/functors placed on separate lines

focus on attempts to move words from bottom to top line

cue: “the boy gave” indicates satisfaction


sentence construction, but moderately impaired comprehension of aural and written language. This dissociation is the more interesting in that the form of the comprehension defect is similar to that found in Broca’s aphasia; i.e., it is asyntactic. However, the basis of MC’s comprehension deficit is certainly not the same as the basis of the Broca patient’s problem.

The pattern of performance for the Broca patient revealed a uniform impairment in all language functions at the level of the processing of syntactic information. That is, the patient was especially impaired in reading function words (words that serve primarily a syntactic function); his production in the story completion task was almost entirely agrammatic; his comprehension was asyntactic and his performance on the sentence anagram task revealed a profound impairment in syntactic organization. This pattern of performance supports the hypothesis that Broca’s aphasia results from a disruption of the syntactic parser of the language processing apparatus (Berndt & Caramazza, 1980; Caramazza & Berndt, 1978; Zurif & Caramazza, 1976). The basis for this claim is that the language component is shown to be affected in all language functions tested (Caramazza & Zurif, 1976; Whitaker, 1971). By this argument, the syntactic parser is not assumed to be impaired in conduction aphasia, even though these patients appear to have asyntactic comprehension, because their performance in other language functions reveals a normally functioning syntactic component.

If we accept that conduction aphasia spares the syntactic parsing device we must look for an explanatory model that places the locus of the disorder at a point between the perceptual processing mechanism (both phonological and graphemic), which appear on the basis of the oral reading task to be functioning relatively normally, and the syntactic and semantic processing systems, which seem to be unimpaired based on performance in the sentence anagram task. Each of the remaining two hypotheses can be elaborated to account for the pattern of MC’s performance in the language tasks reported here.

The decoding deficit hypothesis assumes that the patient can process the input stimulus sufficiently well to recover the phonological and/or the graphemic representations of a word. Beyond this, however, the patient has difficulty carrying out further lexical analysis bearing on the syntactic and semantic properties of the word. The idea here is simply that a less-than-normal lexical representation is formed from a presented word stimulus so that any further processing of the lexical information will be based on an impoverished representation. This hypothesis can explain many of the features that characterize MC’s language performance.

The hypothesis must be developed further, however, if we are to account for the dissociation between his impaired comprehension on the one hand, and his relatively normal speech production and sentence


anagram performance on the other. To explain MC’s asyntactic comprehension, we need to make the assumption that the processing of grammatical morphemes is relatively more impaired than the processing of other lexical forms. This assumption can be motivated on the basis of a linguistic analysis that assigns to grammatical morphemes primarily or exclusively a syntactic description (e.g., Bolinger, 1975; Kimball, 1973, 1975). Thus the representation of function words in the lexicon would be strictly in terms of syntactic description.

By this account, when a patient is presented with a sentence he processes the input at a “normal” level up to the assignment of a phonological description of the input string. Beyond this point, further lexical processing is disturbed in such a way that the internal representation constructed contains less than the normal amount of lexical information ordinarily used in language comprehension. Major lexical items will be more richly specified in the sentence representation because of the dual nature of the information represented in the lexicon (syntactic and semantic). Function words, however, are represented in the lexicon only in terms of their syntactic value and consequently will have a corre- spondingly impoverished status in the representation formed by the patient during the comprehension process. The argument developed here suggests that the conduction patient will construct an internal representation of a sentence that has a relatively more richly specified semantic content than syntactic structure, leading to an exaggerated reliance on lexical-semantic information.

Since by this hypothesis the disorder is specified in terms of lexical processing, it is predicted that the patient should have some difficulty with the story completion task in discerning the type of response he should provide. However, there should not be any impairment in the grammaticality of the selected response. The results we have reported are consistent with this prediction: MC did produce a number of inappropriate responses that reflect his poor comprehension of the story fragment, but the responses produced were grammatically and semantically well formed.

The decoding deficit hypothesis can also explain MC’s performance on the sentence anagram task. The type of processing required in this task combines features of the sentence comprehension and the sentence production tasks. As in the comprehension task, the patient must un- derstand the individual lexical items presented; as in the production task, he must “spontaneously” generate a syntactic frame in which to embed the lexical items presented. Although it is assumed that the lexical processing capacities of the patient are limited, the format of the task allows an adequate level of performance to be achieved, but in a laborious and groping fashion. That is, the lexical information is continuously available in the anagram task, which allows the patient to make use of the im-


poverished representation he can construct by slowly and laboriously arranging and rearranging the words until he has produced a sentence.

To the extent that we accept these arguments to account for performance on the sentence anagram task, we may be undermining our explanation of MC’s asyntactic comprehension in the sentence-picture matching task. In that experiment, the sentence and picture were not presented together but the patient had ample opportunity to study the sentence. It might be expected that under such circumstances the patient could again use a trial-and-error method to construct an adequate internal representation of the sentence. Unfortunately, we have no way of assessing the force of this argument with regard to asyntactic comprehension since semantically reversible sentences cannot meaningfully be used in the sentence anagram task; i.e., both versions would be correct. How- ever, if we consider only comprehension of nonreversible sentences, MC’s performance was very good and at a level comparable to his performance in the anagram task.

The STM deficit hypothesis can also be used as a basis for explaining the language deficits exhibited by MC. This hypothesis predicts that oral reading of single words should be unimpaired since the phonological and semantic components of the system are functioning normally. The finding of asyntactic comprehension is also compatible with this model. It is a basic assumption of all language processing models that normal sentence comprehension requires the functioning of a “working memory” to store the sentence input and/or the results of analyses carried out on the input in the process of assigning a semantic interpretation to the sentence (e.g. Clark & Clark, 1977). A disruption of STM would naturally result in impaired comprehension. To explain the asyntactic form of this comprehension deficit, Saffran and Marin (1975) have argued that the patient with impaired working memory may adopt a strategy of “serial semantic processing” together with a strategy of “assigning syntactic relations in the SVO order” (Bever, 1970). This assumption was developed to account for errors in repetition of reversible passive sentences in the conduction case they studied, and it can also be used to explain poor syntactic comprehension.

There is an implicit assumption in Saffran and Marin’s hypothesis that should be made explicit as it will play a role in our discussion of comprehension failure of visually presented material. The argument that conduction aphasia involves a limitation of the short-term store means that only a limited segment of the sentence input is available in STM at any one time. It is as if we were looking through a narrow window moving along the sentence; what is visible through the window can be seen quite well, but most of the sentence is not available. This is a basic premise of the STM hypothesis; further assumptions concerning serial semantic processing must be motivated on independent grounds since they are not


a logical consequence of the STM deficit hypothesis. Actually, the serial processing assumption is not needed to explain Saffran and Marin’s and Shallice and Butterworth’s (1977) repetition data, nor is it needed to explain our patient’s comprehension.

Saffran and Marin’s implicit assumption is that syntactic processing in real time is not possible with a pathologically limited working memory. Syntactic processing normally requires storing and updating syntactic analysis to the level of a clause (Fodor, Bever, & Garrett, 1974), which exceeds the limitations of the impaired working memory. A consequence, by default, is that the only useful information a patient may have available upon hearing a sentence is the semantic information represented by the major lexical items. Comprehension of a sentence could be based on this lexical-semantic information, together with the SVO strategy suggested by Bever (1970).

MC’s comprehension of visually presented sentences was moderately impaired, even though he had unlimited time to study the stimulus sentences. His asyntactic performance can be explained if we assume that, although MC can perform local syntactic and semantic analyses, he cannot perform a full syntactic analysis on a sentence since this requires the storage in working memory of the output of the local syntactic analyses performed at each point along the sentences. Thus, here again the patient can rely only on the semantic information from major lexical items activated in LTM. Indeed, it is predicted that if the patient has unlimited time to process the sentence he should obtain a very accurate representation of the major lexical items such that the only errors in the sentence-picture matching task should be restricted to syntactic ones. The results obtained here (see Table 13) are largely in agreement with this prediction.

MC’s performance on the sentence anagram task can be explained by assuming that the patient can carry out “local” syntactic analysis within the confines of the “narrow window.” MC performed very well on this task, albeit slowly and in a trial-and-error fashion. Since MC can perform “local” syntactic analyses he can make pair combinations (e.g., Deter- miner + Noun) either serially (e.g., (Determiner + noun) + Aux . . . ) or by first generating pairs (e.g., (Determiner + Noun), (Aux + Verb)) and then linking the pairs by further local analyses at the boundary between pairs (e.g., (Determiner + Noun) + (Aux + Verb)). If the patient were to proceed in this fashion to solve the anagram task, we would expect his performance to be not unlike MC’s, which we have described as effortful and groping.

We have offered two explanations of the language performance of MC that appear to do about equally well in accounting for the obtained results. These explanations should also be evaluated in terms of how


well they can account for the repetition results and, where relevant, other data available in the literature.

GENERAL DISCUSSION

A number of different hypotheses have been proposed to explain the repetition deficit in conduction aphasia. As we have noted in separate discussions of the repetition and language tasks reported here, the performance of MC cannot be accommodated within the classical disconnection hypothesis, nor can it be explained by the encoding deficit hypothesis. These hypotheses cannot provide motivated accounts for performance on the probe task, the differential repetition as a function of mode of presentation, or for the differential effects of form class and delay manipulations on repetition. They are even less successful in explaining MC’s performance on the language tasks, in particular asyntactic comprehension cooccurring with normal syntactic production. However, in light of our remarks about different subgroups within conduction aphasia, it could be maintained that these two hypotheses were developed to explain the behavior of a type of conduction aphasic who is different from our patient. In this case the analyses we have carried out of MC’s performance have little bearing on the validity of the two hypotheses with regard to the range of facts that these models were originally developed to explain. By this argument, however, these two hypotheses lose their status as explanations of “conduction aphasia” in general and must be considered as hypotheses about the nature of the disorder that underlies one subclass of conduction aphasics.

The two other hypotheses we have considered, the decoding deficit and the auditory-verbal STM deficit hypotheses, are moderately successful in accounting for the pattern of results obtained separately in the repetition and language processing tasks. However, if we consider both sets of results we find that the auditory-verbal STM hypothesis continues to provide a reasonable account of MC’s performance, while the decoding deficit hypothesis is confronted with unresolvable conflicts.

There are two major problems that confront the decoding deficit hypothesis. One concerns the patient’s better repetition of visually presented than of aurally presented items. One attempt by Strub and Gardner to deal with this problem is a simple restatement of the results: “visual-semantic connections may be better preserved” (p. 253); in another case they offer a vague appeal to an alternative route for processing visual information. However, even if we were to accept the account they offer for the better performance of repetition of visually presented over aurally presented items, they would still be unable to explain the total pattern of performance of visual and auditory tasks. That is, if it is indeed the case that visual processing is relatively normal, then the


decoding deficit hypothesis would fail to explain our patient’s asyntactic comprehension of visually presented sentences. That is, to explain MC’s performance on the language tasks, particularly his performance on the story completion and reading comprehension tasks, we had to assume that the decoding deficit was a general lexical processing deficit, independent of mode of stimulus input. The decoding deficit hypotheses, to remain internally consistent, necessarily fails to explain one of two major resuts-either the better repetition of visual over auditory inputs, or poor comprehension of visually presented sentences.

The other problem that confronts the decoding deficit hypothesis concerns the very nature of the lexical decoding impairment. Shallice and Warrington (1977) have already objected to the vague claims about lexical decoding disturbances that are assumed to underlie the repetition defect. Indeed, the position that conduction aphasics manifest a lexical processing deficit should be motivated on independent grounds. We have not been able to support this hypothesis in our assessment of MC’s performance on various tasks that require lexical processing. For example, we have reported in this paper that MC’s oral reading performance was excellent. Reading is a complex process that involves both ortho- graphic and phonological processing of lexical forms, and no serious impairments were detected in either of these two processing components. Thus, there is no evidence that MC has a specific lexical decoding deficit that underlies the repetition defect or the asyntactic comprehension we have reported. These objections to the decoding deficit hypothesis are serious enough to rule it out as a possible explanation of the disorder that characterizes our patient’s aphasic performance.

The hypothesis that can best account for MC’s complex performance on repetition and language processing tasks is the auditory-verbal STM deficit hypothesis. The only major result in the repetition tasks that presents some difficulties for the hypothesis is repetition of function words. It appears that MC’s especially marked inability to repeat aurally presented function words is incompatible with the STM hypothesis, un- less we assume that function words are processed differently from other lexical forms. There is some independent evidence that function words and content words are processed differently, at least in sentence production (Garrett, 1973, and it is intuitively obvious that they receive minimal semantic analysis. With regard to MC’s inability to repeat function words when these were presented in phrasal contexts, we need to assume that even in such cases function words are represented only phonologically in short-term store, although they play a crucial role in the syntactic analysis of sentences. By this assumption, aurally presented function words should be especially affected by a disorder of auditory-verbal STM, since the only code of representation available to such lexical forms is the modality in which the impairment is realized.


The STM hypothesis does very well in explaining MC’s performance on the language tasks. This is especially interesting when the complexity of the obtained results is considered. Most important is the fact that the hypothesis can explain the results obtained in the language tasks without recourse to the ad hoc introduction of new mechanisms: the account given is based entirely on consequences of a disruption of short-term memory and the assumptions concerning the processing and representation of function words that were developed to explain the repetition results.

One elaboration of the STM deficit hypothesis that was needed to explain the language comprehension performance of our patient was the claim that MC could apply his unimpaired syntactic knowledge only to a small segment of the presented material at a time. In particular, it was assumed that MC could apply local analyses-analyses between pairs of words-but could not make use of working memory to store the output of syntactic analysis. This assumption, which follows naturally from the hypothesis of pathologically reduced capacity in the STM store, predicts MC’s asyntactic comprehension of sentences.

To conclude, we have reported an extensive analysis of the repetition and language processing performance of a conduction aphasic. Of the four hypotheses considered, the only one that could provide a motivated account of all the major features of performance was the auditory-verbal STM deficit hypothesis. If our analysis is correct, we have provided a strong demonstration of the relationship between a nonlinguistic processing component and particular aphasic symptoms in a patient. The study of patients of this type should be especially fruitful for an analysis of the contribution of auditory-verbal STM to various language functions.

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